الفهرس 
Acknowledgement
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Abstract
This work studied the effect of maternal induced hypothyroidism on the development of rat visual cortex postnatally and the therapeutic effect of thyroid hormone replacement therapy.
A total number of 60 female albino rats were used and divided equally into 3 groups. The 1stgroup was considered as a control group, they were given distilled water daily from the gestational day 1 until the postnatal day 21. The 2ndgroup was subjected to antithyroid drug (carbimazole) in order to induce hypothyroid state in a dose of 5mg/day/rat. The drug was administered through an intragastric intubation daily from the gestational day 1 until the postnatal day 21. The 3rd group was given carbimazole orally through an intragastric intubation daily from the gestational day 1 until the postnatal day 21in a dose of 5 mg/day/pregnant rat, and eltroxin from gestational day 10 until postnatal day 21 in a dose of 5µg/day/rat in 1ml 0.09 NaCl subcutaneously. Offspring from all groups were sacrificed at the following ages: newborn, 5, 10 and 20 days.
Brains were extracted; some brain specimens were fixed in Bouin’s fluid and then processed for paraffin blocks and light microscopic examination. Other brain specimens were fixed in gluteraldehyde in order to be examined by the electron microscope. Sagittal sections were done. These samples were subjected to Gallocyaninchrom-alum stain for Nissl granules, nuclei and nucleoli as well as semithinsectining and ultrathin sectioning to study the ultrastructure of the visual cortex. The postnatal developmental changes were studied in normal group and the two experimental groups.
This study showed that the development of rat visual cortex is completed by the third week postnatally when the neurons achieve their mature appearance as indicated by increased size of cell body and nuclei. Also there were an increase in the depth of the cortical layers and a reduction in the packing of cells and their arrangement in clusters. The results showed that the cellular component of the deep layer (V) reached maturity before those of the superficial layers (II\III).
The results showed that maternal hypothyroidism induced a delayed growth and differentiation of the visual cortex. This was noted by a reduction in the thickness of the cortical layers, decreased nuclear size and increase in packing of cells due to delay in the dendritic maturation of the neurons. Multiple darkly stained cells were noticed that indicated enhanced apoptosis. Loss of clustering pattern of large pyramidal cells of ganglionic layer (layer V) was observed. Borders between layers couldn’t be easily distinguished.
Treatment with levothyroxine resulted in attenuating the alterations induced by hypothyroidismwith normal appearance of the majority of cells. Few cells showed residual damage.
Conclusion:
This work could explain the important role of thyroid hormone on the processes that take place during fetal development such as cell proliferation and migration, that affect the cytoarchitecture of the visual cortex. Any situation resulting in a decreased availability of T4 to fetal brain is harmful for neurodevelopment. Early discovering of hypothyroidism in pregnant women and thyroid hormone replacement therapy should be reconsidered in order to compensate for thyroid hormone deficiency during pregnancy.
It is recommended to treat overt hypothyroidism as soon as detected during pregnancy, because normal thyroid hormone level is needed for pregnancy and normal foetal brain development. If hypothyroidism has been diagnosed before pregnancy and is being treated with levothyroxine, dose adjustment will be needed during pregnancy.
The experimental work herein will require additional studies on the effect of maternal induced hypothyroidism on the synaptogenesis in the primary visual cortex. Further studies to determinethe reversibility of these changes that occureddue to maternal induced hypothyroidism in the adult age will be needed.